A large number of experimental studies has demonstrated that angiotensin II (Ang II) is involved in key events of the inflammatory process. This study aimed to evaluate the role of Ang II type 1 (AT1) and Ang II type 2 (AT2) receptors on periodontitis. Methods: Experimental periodontitis was induced by placing a 5.0 nylon thread ligature around the second upper left molar of AT1 mice, no-ligature or ligature (AT1-NL and AT1-L), AT2 (AT2-NL or AT2-L) and wild type (WT-NL or L). Alveolar bone loss was scanned using Micro-CT. Cytokines, peptides and enzymes were analyzed from gingival tissues by Elisa and RT-PCR. Results: The blockade of AT1 receptor resulted in bone loss, even in healthy animals. Ang II receptor blockades did not prevent linear bone loss. Ang II and Ang 1-7 levels were significantly increased in the AT2-L (p < 0.01) group compared to AT2-NL and AT1-L. The genic expression of the Mas receptor was significantly increased in WT-L and AT2-L compared to (WT-NL and AT2-NL, respectively) and in AT1-L. Conclusions: Our data suggest that the receptor AT1 appears to be important for the maintenance of bone mass. AT2 receptor molecular function in periodontitis appears to be regulated by AT1.

Background: The aim of this study was to evaluate the role of AT1 and AT2 receptors in a periodontal inflammation experimental model. Methods: Periodontal inflammation was induced by LPS/Porphyromonas gingivalis. Maxillae, femur, and vertebra were scanned using Micro-CT. Maxillae were analyzed histopathologically, immunohistochemically, and by RT-PCR. Results: The vertebra showed decreased BMD in AT1 H compared with WT H (p < 0.05). The femur showed increased Tb.Sp for AT1 H and AT2 H, p < 0.01 and p < 0.05, respectively. The Tb.N was decreased in the vertebra (WT H-AT1 H: p < 0.05; WT H-AT2 H: p < 0.05) and in the femur (WT H-AT1 H: p < 0.01; WT H-AT2 H: p < 0.05). AT1 PD increased linear bone loss (p < 0.05) and decreased osteoblast cells (p < 0.05). RANKL immunostaining was intense for AT1 PD and WT PD (p < 0.001). OPG was intense in the WT H, WT PD, and AT2 PD when compared to AT1 PD (p < 0.001). AT1 PD showed weak immunostaining for osteocalcin compared with WT H, WT PD, and AT2 PD (p < 0.001). AT1 H showed significantly stronger immunostaining for osteonectin in fibroblasts compared to AT2 H (p < 0.01). Conclusion: AT1 receptor knockout changed bone density, the quality and number of bone trabeculae, decreased the number of osteoblast cells, and increased osteonectin in fibroblasts.

The aim of this study was to investigate the effect of thermogenic supplementation on the bone tissue of rats subjected to orthodontic movement. A total of 38 male Wistar rats underwent orthodontic movement of the left permanent maxillary first molars for 21 days. The rats were assigned to three groups: Control group: water; Thermogenic 1: C4 Beta Pump thermogenic; or Thermogenic 2: PRE-HD/Pre-workout. Micro-computed tomography (micro-CT) was used to investigate the dynamic changes in the microstructure of alveolar bone during orthodontic tooth movement in rats. Histopathologic analysis was performed by hematoxylin and eosin (H&E) staining, whereas tartrate-resistant acid phosphatase (TRAP) was employed for osteoclast count. Maxillary tissue was collected and evaluated by immunohistochemistry for receptor activator of NF-κB (RANK), receptor activator of NF-κB ligand (RANKL), and osteoprotegerin (OPG). The Thermogenic 2 group exhibited a significantly lower percentage of bone volume fraction (BV/TV) (68.21% ± 17.70%) compared to the control (86.84% + 12.91%) and Thermogenic 1 groups (86.84% + 15.94%) (p < 0.05). The control group had a significantly higher mean orthodontic movement in the mesial direction (0.2143 mm + 0.1513 mm) than the Thermogenic 2 group (0.0420 mm + 0.05215 mm) (p < 0.05). The Thermogenic 2 and Thermogenic 1 groups showed a stronger immunostaining for RANKL when compared to the control group (p < 0.05). The supplementation used in the Thermogenic 2 group (PRE-HD/Pre-workout) induced alveolar bone loss in rats subjected to orthodontic movement, which can be related to the regulation of the RANK/RANKL/OPG signaling pathway. This suggests the influence of thermogenic supplements on bone metabolism seems to depend on their composition.